The present invention relates to systems and methods for correcting deficiencies that may arise in the operation of the human heart, specifically in the operation of valves in the human heart.
An understanding of the human heart, and of deficiencies that may arise in the human heart, may be better understood with reference to the accompanying drawings, FIG. 1 and FIG. 2.
FIG. 1 shows a sectional view of the heart 10 of a human subject. The mitral valve 12 is located between the left atrium 14 and left ventricle 16, generally adjacent to the aortic valve 18. The papillary muscles 20, 22 are finger-like muscular projections that extend from the wall of the left ventricle, as shown. Inelastic tendons, known as the chordae tendineae 24 extend from the antero-lateral papillary muscle 20 and from the postero-medial papillary muscle 22 to the anterior leaflet 26 and posterior leaflet 28 of the mitral valve 12, as shown. In a healthy heart, the point of connection between the antero-lateral papillary muscle 20 is at a level marked as P0 in FIG. 1. When connected at this level in relation to the rest of the heart, the papillary muscle(s) serve, in part, to limit movement of the mitral and tricuspid valve leaflets. During the diastolic phase of the cardiac cycle, the left ventricular myocardium relaxes, thus causing the pressure within the left ventricle to decrease and causing the mitral valve leaflets to open as blood travels from the left atrium into the left ventricle. Thereafter, during the systolic phase of the cardiac cycle, the left ventricle contracts, thereby causing an increase in pressure within the left ventricle. This increase in left ventricular pressure causes the mitral valve leaflets 26, 28 to coapt and close. Concurrently with contraction of the left ventricle, the papillary muscles also contract causing the chordae tendineae to tighten. When the point of connection between the chordae tendineae and the papillary muscle are located at level P0 as shown in FIG. 1, then the tightened chordae tendineae hold the mitral valve leaflets in the proper position for closure of the valve and prevents the mitral valve leaflets from prolapsing through the valve annulus.
Mitral valve regurgitation (also known as mitral insufficiency or mitral incompetence) results when the leaflets of the mitral valve do not fully coapt (i.e., do not close tightly), thus allowing blood to backflow from the left ventricle 16 into the left atrium during the systolic phase of the cardiac cycle. This can result in decreased cardiac output and inadequate perfusion of tissues throughout the body, with various resultant symptoms, including severe fatigue and shortness of breath.
Mitral regurgitation can result from a number of causes. In some cases, mitral regurgitation may result from shortening of one or both of the papillary muscles due to a prior myocardial infarction or cardiomyopathy. Also, in some cases, papillary muscles may shorten due to scar tissue formation in patients who have undergone a type of surgical procedure (i.e., endocardial resection) for the treatment of ventricular arrhythmias. Again, the papillary muscles themselves may be displaced downwardly as a result of ischemic distortion in the wall of the heart, with the result that the cordeae pull down on the leaflets with the same effect as being shortened. When the papillary muscles are shortened or moved, the chorda tendonae may create more traction on the mitral valve leaflets, preventing the leaflets from closing properly during the systolic phase of the cardiac cycle. In some cases, mitral regurgitation may result from the dilation of left ventricular wall to which the papillary muscle is directly attached. In such cases, the left ventricular wall bellows out and causes the papillary muscle/chordae apparatus to be in tension, thereby preventing leaflets from fully coapting. FIG. 2 exemplifies the effect described above where, in the case exemplified, the wall of the heart has moved downward relative to the rest of the heart due to ischemic distortion. Thus, here, the point of connection between the chordae tendineae and the papillary muscle has fallen to the level shown by the mark at P1 in relation to the rest of the heart, from the level at P0 where it was positioned when in full health. As a result, the posterior leaflet 28 has been pulled downwards by about the same amount, thereby preventing the leaflets from coapting during systole.
The prior art has included a number of surgical and interventional procedures aimed at treating mitral regurgitation by lengthening papillary muscle(s) or chordae tendineae. For example, some systems in the prior art describe a system and method for elongating a papillary muscle by attaching a muscle elongating device to the papillary muscle.
Other systems in the prior art describe methods, devices, and systems for the endovascular repair of cardiac valves (particularly the atrioventricular valves and most particularly the mitral valve) wherein interventional tools, catheters and other equipment are advanced though the vasculature and to the heart chambers. The interventional tools and other equipment are then used to modify the valve leaflets, the valve annulus, the chordae tendineae and/or the papillary muscles to improve closure of the mitral valve leaflets.
Further systems describe devices and methods for treatment of mitral regurgitation by deployment of implantable devices within the anterior and posterior interventricular veins, or only in the posterior interventricular vein, to cause medial displacement of the anterior and posterior interventricular veins towards the left ventricular cavity. This in turn causes repositioning of the papillary muscles in a manner that purportedly brings the mitral valve leaflets into proper coaptation during the systolic phase of the cardiac cycle.
Further, United States Patent Application Publication No. 20080269876 describes a system and method for implanting devices and fillers within the papillary muscle itself, with the purpose of “bulking up” the papillary muscle, with the intention of lifting the points of connection of the chordae tendineae. Yet each of these solutions includes disadvantages and further deficiencies. For example the system of implanting a filler within the papillary muscle may itself sometimes result in further lowering the points of connection of the chordae tendineae to papillary muscle, thereby exacerbating the problem and further preventing coaptation of the leaflets.
Thus, there remains a need for the development of new devices and methods for altering the length and/or position of a papillary muscle so as to improve the function of cardiac valves to which the papillary muscle is attached. The present invention addresses these and other needs.